Palmar plantar erythrodysesthesia differential diagnosis: Difference between revisions

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* Positive Koebner phenomenon
* Positive Koebner phenomenon
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| style="background: #DCDCDC; padding: 5px; text-align: left;" valign="top" | '''[[Dyshidrotic eczema]]'''
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* Deep-seated clear vesicles; later, scaling, fissures and lichenification occur
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* Deep-seated vesicles or blisters on the tips and lateral sides of the fingers, palms, and soles with subsequent scaling, fissures and lichenificatoin
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* Acute:
:* intraepidermal spongiotic vesicles or bullae that do not involve the intraepidermal portion of the eccrine sweat duct (acrosyringium).
:* A sparse, superficial perivascular infiltrate of lymphocytes
* Chronic:
:* Predominance of parakeratosis and acanthosis with minimal or no spongiosis and a dermal lymphocytic infiltrate.
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* Intensely pruritic
* History of recurrence
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Revision as of 23:14, 30 July 2019

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mandana Chitsazan, M.D. [2]

Overview

PPE must be differentiated from Graft-Versus-Host Disease (GVHD).

Differentiating palmar plantar erythrodysesthesia from other Diseases

Disease Clinical manifestation Histopathology Additional diagnostic clues
Palmar plantar erythrodysesthesia
  • The areas of well-defined intense erythema and edema
  • A variable degree of epidermal (keratinocytes) necrosis
  • Vacuolar degeneration of the basal cell layer of epidermis
  • Spongiosis
  • Hyperkeratosis
  • Lymphohistiocytic infiltrates
  • Superficial perivascular infiltration of dermis by lymphocytes and eosinophils
  • Papillary dermal edema
  • Neutrophilic eccrine hidradenitis
  • Eccrine squamous syringometaplasia, in severe PPE (WHO grades 3 and 4)
  • History of chemotherapeutic agent use
Graft-versus-host disease
  • A diffuse macular erythema whihich may form papules
  • Histologic features of Graft-versus-host disease and palmar plantar erythrodysesthesia are identical in early stages and serial biopsies may be needed to distinguish these two entities.
  • Features suggestive of Graft-versus-host disease:
  • Degenerate keratinocytes at all levels of the epidermis
  • Adjacent lymphocytes (satellite cell necrosis)
  • Extracutaneous manifestations of AGVHD, including:
  • Gastrointestinal symptoms such as diarrhea and abdominal pain
  • Elevated liver enzymes
Contact dermatitis
  • Well-demarcated, eczematous eruptions localized to the area of skin that in contact with the culprit allergen
  • Acute eruption: vesicular
  • Chronic eruption: lichenified and scaly plaques
  • Eosinophilic spongiosis
  • Exocytosis of eosinophils and lymphocytes
  • History of allergen exposure
  • Pruritic lesions
  • Patch testing may help to identify allergens
Palmoplantar plaque psoriasis
  • Sharply defined erythematous, scaly plaques on the palms and/or soles
  • Fissures
  • Acanthosis
  • Hyperkeratosis
  • Parakeratosis
  • Neutrophilic infiltration in the epidermis and stratum corneum (Kogoj pustules and Munro's microabscesses)
  • Abundant mononuclear cells (mainly myeloid cells and T cells) in the dermis
  • Pruritus is common
  • Positive Koebner phenomenon
Dyshidrotic eczema
  • Deep-seated clear vesicles; later, scaling, fissures and lichenification occur
  • Deep-seated vesicles or blisters on the tips and lateral sides of the fingers, palms, and soles with subsequent scaling, fissures and lichenificatoin
  • Acute:
  • intraepidermal spongiotic vesicles or bullae that do not involve the intraepidermal portion of the eccrine sweat duct (acrosyringium).
  • A sparse, superficial perivascular infiltrate of lymphocytes
  • Chronic:
  • Predominance of parakeratosis and acanthosis with minimal or no spongiosis and a dermal lymphocytic infiltrate.
  • Intensely pruritic
  • History of recurrence
x1 x2 x3 x4

References